Endocrinology — MCQs
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A 30-year-old female presents with a 3-month history of 10kg weight loss despite an increased appetite. She also complains of anxiety, diarrhea, and amenorrhea. Examination reveals a fine tremor, brisk reflexes, and a systolic murmur heard throughout the precordium. A urine pregnancy screen was negative. What is the most likely finding on examining the pulse?
What is a common clinical manifestation of adrenal insufficiency?
Which of the following findings is most consistent with the diagnosis of subacute (De Quervain's) thyroiditis?
A 53-year-old woman with metastatic breast cancer presents with lethargy, fatigue, and hypercalcemia, leading to a near-comatose state. After addressing airway, breathing, and circulation, what is the best initial therapy for this patient's hypercalcemia?
Which of the following factors determines whether a patient develops acromegaly or gigantism?
True about Chvostek's sign are all of the following except?
A 20-year-old male presents with chronic constipation, headache, characteristic habitus, neuromas of the tongue, medullated corneal nerve fibers, and a 2x2 cm nodule in the left lobe of the thyroid. What is the most likely diagnosis?
A 30-year-old pregnant woman presents for a routine physical examination. Her plasma levels of TSH are high, but her total thyroid hormone concentration is normal. Which of the following best reflects the patient's clinical state?
Which of the following statements regarding thyrotoxicosis are true?
What is the most common presentation of endemic goiter?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 101: A 30-year-old female presents with a 3-month history of 10kg weight loss despite an increased appetite. She also complains of anxiety, diarrhea, and amenorrhea. Examination reveals a fine tremor, brisk reflexes, and a systolic murmur heard throughout the precordium. A urine pregnancy screen was negative. What is the most likely finding on examining the pulse?
- A. Pulsus paradoxus
- B. Collapsing pulse
- C. Irregularly irregular pulse (Correct Answer)
- D. Pulsus alternans
Explanation: The clinical presentation of weight loss despite increased appetite, anxiety, diarrhea, and amenorrhea in a young female is classic for **Hyperthyroidism** (likely Graves' disease) [1], [4]. The presence of a fine tremor, brisk reflexes, and a hyperdynamic precordium further supports this diagnosis [1]. **Why the correct answer is right:** Hyperthyroidism induces a hyperadrenergic state, increasing the sensitivity of the heart to catecholamines. This frequently leads to supraventricular tachyarrhythmias, most notably **Atrial Fibrillation (AF)** [2]. AF is characterized by an **irregularly irregular pulse** and a pulse deficit. While sinus tachycardia is the most common rhythm abnormality in thyrotoxicosis, AF occurs in approximately 10–15% of patients, especially if the hyperthyroidism is severe or long-standing [2], [3]. **Why the incorrect options are wrong:** * **Pulsus paradoxus:** Defined as an inspiratory drop in systolic BP >10 mmHg; it is seen in cardiac tamponade, severe asthma, or COPD. * **Collapsing pulse (Water-hammer pulse):** Associated with high-output states (like hyperthyroidism) and Aortic Regurgitation. While hyperthyroidism *can* cause a wide pulse pressure [1], the NEET-PG focus for "most likely finding" in the context of rhythm/examination often points toward the arrhythmia (AF). * **Pulsus alternans:** Alternating strong and weak beats; it is a hallmark of severe Left Ventricular Failure. **High-Yield Clinical Pearls for NEET-PG:** * **Most common arrhythmia in Hyperthyroidism:** Sinus Tachycardia [2]. * **Most common chronic arrhythmia in Hyperthyroidism:** Atrial Fibrillation [3]. * **Treatment of choice for symptoms:** Beta-blockers (Propranolol) as they inhibit peripheral conversion of T4 to T3 and control adrenergic symptoms [3], [5]. * **Auscultation:** A systolic murmur in hyperthyroidism is often a "Flow Murmur" due to the hyperdynamic circulation.
Question 102: What is a common clinical manifestation of adrenal insufficiency?
- A. A rise in plasma sodium/potassium ratio
- B. Low blood pressure (Correct Answer)
- C. Increased breakdown of protein
- D. All of the above
Explanation: Adrenal insufficiency (Addison’s disease) results from the inadequate production of adrenocortical hormones, primarily **aldosterone** and **cortisol** [1]. **Why "Low blood pressure" is correct:** Hypotension is a hallmark of adrenal insufficiency [2]. It occurs due to two main mechanisms: 1. **Mineralocorticoid deficiency:** Lack of aldosterone leads to renal wasting of sodium and water, causing hypovolemia [2]. 2. **Glucocorticoid deficiency:** Cortisol is essential for maintaining vascular tone; its absence results in decreased sensitivity of blood vessels to catecholamines, leading to vasodilation and hypotension [3]. **Why the other options are incorrect:** * **A. A rise in plasma sodium/potassium ratio:** In adrenal insufficiency, aldosterone deficiency leads to **hyponatremia** (low sodium) and **hyperkalemia** (high potassium). Therefore, the Na+/K+ ratio actually **decreases**, not increases [1]. * **C. Increased breakdown of protein:** Cortisol is a catabolic hormone that promotes protein breakdown (proteolysis) to provide substrates for gluconeogenesis. In adrenal insufficiency, there is a **deficiency** of cortisol, leading to decreased protein catabolism compared to states of cortisol excess (like Cushing’s syndrome). **High-Yield Clinical Pearls for NEET-PG:** * **Hyperpigmentation:** Seen only in *primary* adrenal insufficiency due to increased ACTH (and its precursor POMC), which stimulates melanocytes [2]. * **Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Diagnosis:** The gold standard is the **ACTH Stimulation Test** (Cosyntropin test) [2]. * **Adrenal Crisis:** An acute emergency characterized by profound hypotension/shock, often precipitated by stress or infection in a patient with chronic insufficiency [2]. Treatment requires immediate IV hydrocortisone and fluid resuscitation.
Question 103: Which of the following findings is most consistent with the diagnosis of subacute (De Quervain's) thyroiditis?
- A. A 45-year-old female with a 2-week history of a painful thyroid gland, elevated T4 and T3, low TSH, and increased radioactive iodine uptake (RAIU).
- B. A 25-year-old female with a painless enlarged thyroid, elevated T4 and T3, undetectable TSH, and increased RAIU.
- C. A 45-year-old female with fatigue, low T4 and T3, and low TSH.
- D. A 45-year-old male with a painful thyroid of 8 weeks duration, low free T4 and T3, and elevated TSH. (Correct Answer)
Explanation: Explanation: Subacute (De Quervain’s) thyroiditis is a granulomatous inflammatory condition, typically following a viral upper respiratory infection. Its clinical course is characteristically triphasic: 1. Thyrotoxic phase (early): Inflammation causes the release of preformed hormones (high T3/T4, low TSH). 2. Hypothyroid phase (intermediate): Depletion of hormone stores leads to transient hypothyroidism (low T3/T4, high TSH). 3. Euthyroid phase (recovery): Restoration of normal gland function. The correct answer describes a patient in the hypothyroid phase (8 weeks duration). The hallmark of De Quervain’s is a painful, tender thyroid accompanied by a markedly elevated ESR and low radioactive iodine uptake (RAIU) due to follicular cell damage [2]. Analysis of Options: * Option A: Incorrect. While the pain and thyrotoxic labs fit the early phase, the RAIU must be low in thyroiditis (leakage, not overproduction) [3]. Increased RAIU suggests Graves' disease or toxic nodules. * Option B: Incorrect. Painless enlargement with high RAIU is classic for Graves' disease [1]. * Option C: Incorrect. Low T4/T3 with low TSH indicates Secondary (Central) Hypothyroidism, not a primary thyroid pathology [4]. * Option D (Correct): Correct. Represents the hypothyroid phase of subacute thyroiditis. The pain persists or is resolving, and the labs reflect the temporary exhaustion of thyroid hormone stores [2]. NEET-PG High-Yield Pearls: * Diagnosis: Clinical (tender gland) + High ESR + Low RAIU [2]. * Pathology: Giant cells and granulomatous inflammation on biopsy. * Treatment: NSAIDs for mild cases; Steroids for severe pain. Beta-blockers for the thyrotoxic phase (Antithyroid drugs like Carbimazole are not effective as there is no new hormone synthesis) [2].
Question 104: A 53-year-old woman with metastatic breast cancer presents with lethargy, fatigue, and hypercalcemia, leading to a near-comatose state. After addressing airway, breathing, and circulation, what is the best initial therapy for this patient's hypercalcemia?
- A. Bisphosphonates
- B. IV estrogen therapy
- C. Saline infusion and furosemide (Correct Answer)
- D. Vitamin D
Explanation: The patient presents with **Hypercalcemic Crisis** (lethargy, near-comatose state), likely secondary to bone metastasis from breast cancer. In severe hypercalcemia (typically Calcium >14 mg/dL), the priority is rapid volume expansion and enhancement of urinary calcium excretion. **Why Option C is correct:** * **Saline Infusion:** Patients with severe hypercalcemia are invariably dehydrated due to polyuria (nephrogenic diabetes insipidus) and vomiting. **Isotonic saline (0.9% NaCl)** is the first-line treatment to restore intravascular volume and increase the glomerular filtration rate (GFR) [3]. Severe life-threatening hypercalcemia is often due to dehydration and should be managed medically with intravenous fluids [2]. * **Furosemide:** Once the patient is euvolemic, loop diuretics like furosemide are added to inhibit calcium reabsorption in the thick ascending limb of the Loop of Henle, further promoting calciuresis. *Note: Furosemide should never be given before volume resuscitation as it can worsen dehydration.* **Why other options are incorrect:** * **A. Bisphosphonates (e.g., Zoledronic acid):** While these are the mainstay for long-term management of malignancy-associated hypercalcemia, they take **24–72 hours** to reach peak effect [1]. They are not suitable as the *sole initial* therapy in an emergency. * **B. IV Estrogen:** Estrogen has no role in the acute management of hypercalcemia; in fact, selective estrogen receptor modulators can sometimes worsen hypercalcemia in breast cancer patients (flare reaction). * **D. Vitamin D:** This would exacerbate hypercalcemia by increasing intestinal calcium absorption and bone resorption. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common cause of hypercalcemia:** Outpatient = Primary Hyperparathyroidism; Inpatient = Malignancy. 2. **ECG Finding:** Shortened QT interval is a classic sign of hypercalcemia. 3. **Refractory Cases:** If saline and bisphosphonates fail, or in patients with renal failure, **Hemodialysis** is the treatment of choice. 4. **Calcitonin:** Can be used alongside saline for a rapid (but short-lived) reduction in calcium while waiting for bisphosphonates to kick in.
Question 105: Which of the following factors determines whether a patient develops acromegaly or gigantism?
- A. Sex
- B. Age at onset of the tumor (Correct Answer)
- C. Amount of available calcium
- D. Degree of function of the tumor
Explanation: The clinical manifestation of growth hormone (GH) excess is primarily determined by the **status of the epiphyseal plates** at the time of onset [1]. ### Why the Correct Answer is Right: * **Gigantism:** Occurs when GH hypersecretion begins **before the fusion of the epiphyses** (pre-pubertal) [1]. Excessive GH stimulates the open growth plates of long bones, leading to dramatic longitudinal growth and tall stature [1]. * **Acromegaly:** Occurs when GH hypersecretion begins **after the fusion of the epiphyses** (post-pubertal) [1]. Since longitudinal growth is no longer possible, the excess GH causes appositional bone growth (thickening), leading to characteristic features like frontal bossing, enlarged hands/feet (acral enlargement), and macroglossia [1]. ### Why Other Options are Wrong: * **Sex:** GH excess affects both males and females similarly; gender does not dictate the clinical entity (gigantism vs. acromegaly). * **Amount of available calcium:** While GH affects bone metabolism, calcium levels do not determine the pattern of skeletal growth. * **Degree of function of the tumor:** The quantity of GH produced influences the severity of symptoms, but the *type* of skeletal deformity is strictly dependent on whether the bones are still capable of linear growth [1]. ### High-Yield Clinical Pearls for NEET-PG: * **Most common cause:** Somatotroph adenoma of the anterior pituitary. * **Best Screening Test:** Serum **IGF-1** levels (more stable than pulsatile GH) [2]. * **Confirmatory Test:** Oral Glucose Tolerance Test (**OGTT**) – failure to suppress GH below 1 ng/mL (or 0.4 ng/mL in newer assays) after 75g glucose [2]. * **Most common cause of death:** Cardiovascular disease (specifically cardiomyopathy). * **Associated condition:** Increased risk of **Colonic Polyps** and Adenocarcinoma [2].
Question 106: True about Chvostek's sign are all of the following except?
- A. Denotes neuromuscular hyperexcitability
- B. Elicited over the face
- C. Raised calcium level (Correct Answer)
- D. Facial nerve is stimulated by tapping
Explanation: Chvostek’s sign is a clinical indicator of latent tetany resulting from hypocalcemia (low serum calcium levels) [1]. 1. Why Option C is correct: The statement "Raised calcium level" is false. Chvostek’s sign is elicited when serum calcium levels are low. In hypocalcemia, the threshold for nerve depolarization is lowered, leading to neuromuscular hyperexcitability. High calcium levels (hypercalcemia) actually decrease neuromuscular excitability [1]. 2. Why other options are incorrect: * Option A: Hypocalcemia increases the permeability of neuronal membranes to sodium ions, causing spontaneous discharges or neuromuscular hyperexcitability. * Option B & D: The sign is elicited over the face by tapping the facial nerve at the angle of the jaw (anterior to the external auditory meatus). A positive result is characterized by twitching of the ipsilateral facial muscles (nose, mouth, or eye). High-Yield Clinical Pearls for NEET-PG: * Trousseau’s Sign: A more sensitive and specific sign for hypocalcemia than Chvostek’s. It involves inflating a BP cuff above systolic pressure for 3 minutes, resulting in carpopedal spasm (flexion of wrist/MCP joints, extension of IP joints, adduction of thumb). * Causes of Hypocalcemia: Hypoparathyroidism (often post-thyroidectomy), Vitamin D deficiency, Acute Pancreatitis, and Hypomagnesemia [1]. * False Positives: Chvostek’s sign can be present in approximately 10% of healthy individuals with normal calcium levels. * Management: Acute symptomatic tetany is treated with IV Calcium Gluconate.
Question 107: A 20-year-old male presents with chronic constipation, headache, characteristic habitus, neuromas of the tongue, medullated corneal nerve fibers, and a 2x2 cm nodule in the left lobe of the thyroid. What is the most likely diagnosis?
- A. Sporadic medullary carcinoma of the thyroid
- B. Familial medullary carcinoma of the thyroid
- C. Multiple Endocrine Neoplasia (MEN) type 2A
- D. Multiple Endocrine Neoplasia (MEN) type 2B (Correct Answer)
Explanation: ### Explanation The correct diagnosis is **Multiple Endocrine Neoplasia (MEN) type 2B**. This syndrome is characterized by the triad of Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, and a distinct physical phenotype. **Why Option D is correct:** The patient exhibits pathognomonic features of MEN 2B: * **Mucosal Neuromas:** Present on the tongue, lips, and eyelids. * **Marfanoid Habitus:** Long limbs and characteristic body proportions (implied by "characteristic habitus"). * **Medullated Corneal Nerve Fibers:** A highly specific finding for MEN 2B. * **Gastrointestinal involvement:** Chronic constipation in these patients is often due to **intestinal ganglioneuromatosis**, which affects gut motility. * **Thyroid Nodule:** Represents Medullary Thyroid Carcinoma (MTC), which occurs in nearly 100% of these patients and is often aggressive [2]. **Why other options are incorrect:** * **Option A & B:** While MTC is present in both sporadic and familial forms, these do not present with marfanoid habitus, mucosal neuromas, or medullated corneal nerves. * **Option C (MEN 2A):** MEN 2A consists of MTC, Pheochromocytoma, and Parathyroid Hyperplasia. It lacks the mucosal neuromas and marfanoid features seen in MEN 2B [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Both MEN 2A and 2B are caused by germline mutations in the **RET proto-oncogene** [2]. * **MTC Aggression:** MTC in MEN 2B is more aggressive and occurs earlier than in MEN 2A; prophylactic thyroidectomy is often recommended in infancy [2]. * **Screening:** Always rule out **Pheochromocytoma** (check urinary metanephrines) before performing thyroid surgery to prevent a hypertensive crisis [1], [2]. * **MEN 2B Components:** MTC (100%), Pheochromocytoma (50%), Mucosal Neuromas/Marfanoid habitus (100%), and *rarely* Hyperparathyroidism (unlike MEN 2A).
Question 108: A 30-year-old pregnant woman presents for a routine physical examination. Her plasma levels of TSH are high, but her total thyroid hormone concentration is normal. Which of the following best reflects the patient's clinical state?
- A. Graves' disease
- B. Hashimoto's disease (Correct Answer)
- C. A pituitary tumor secreting TSH
- D. A hypothalamic tumor secreting thyrotropin-releasing hormone (TRH)
Explanation: The patient presents with **elevated TSH** and **normal total thyroid hormone** levels. In pregnancy, high estrogen levels increase **Thyroxine-Binding Globulin (TBG)**, which normally leads to an increase in *total* T4/T3 to maintain normal *free* hormone levels. A "normal" total T4 in a pregnant patient is often inappropriately low, suggesting an underlying inability of the thyroid gland to meet the increased physiological demand. 1. **Why Hashimoto’s Disease is correct:** This clinical picture (High TSH, Normal/Low-Normal T4) represents **Subclinical Hypothyroidism** [1]. Hashimoto’s thyroiditis is the most common cause of primary hypothyroidism. In the early stages, the pituitary compensates for a failing thyroid by increasing TSH production to maintain thyroid hormone levels within the reference range [1]. 2. **Why the other options are incorrect:** * **Graves’ Disease:** Characterized by hyperthyroidism. TSH would be suppressed (low), and thyroid hormones (T4/T3) would be elevated [1]. * **Pituitary/Hypothalamic Tumors (Options C & D):** These cause **Secondary Hyperthyroidism**. While TSH would be high, the thyroid hormones (T4/T3) would also be significantly **elevated**, not normal, as the thyroid gland is being overstimulated [1]. **NEET-PG High-Yield Pearls:** * **Pregnancy & Thyroid:** Total T4/T3 levels increase by 1.5 times due to increased TBG. Therefore, a "normal" total T4 in pregnancy may actually indicate hypothyroidism. * **Subclinical Hypothyroidism:** Defined as Elevated TSH with Normal Free T4 [1]. * **Wolff-Chaikoff Effect:** Transient hypothyroidism caused by an iodine load (relevant as Hashimoto's patients are sensitive to iodine). * **Treatment Goal:** In pregnancy, TSH should ideally be maintained <2.5 mIU/L to prevent maternal and fetal complications.
Question 109: Which of the following statements regarding thyrotoxicosis are true?
- A. Statements 1 and 2 are true, while statements 3, 4, and 5 are false.
- B. Statements 3 and 4 are true, while statements 1, 2, and 5 are false.
- C. Statements 1, 2, 3, and 4 are true, while statement 5 is false. (Correct Answer)
- D. Statements 4 and 5 are true, while statements 1, 2, and 3 are false.
Explanation: **Explanation** Thyrotoxicosis refers to the clinical syndrome of hypermetabolism resulting from elevated circulating free T4 and/or T3. Understanding the distinction between hyperthyroidism (excess synthesis) and other causes of thyrotoxicosis is crucial for NEET-PG. **Analysis of Statements:** 1. **Statement 1 (True):** Thyrotoxicosis is defined as the state of thyroid hormone excess [1]. 2. **Statement 2 (True):** Hyperthyroidism is a subset of thyrotoxicosis caused specifically by **thyroid gland hyperactivity** (e.g., Graves' disease, Toxic Multinodular Goiter) [2]. 3. **Statement 3 (True):** Thyrotoxicosis can occur without hyperthyroidism, such as in **Subacute Thyroiditis** (leakage of preformed hormone) or **Thyrotoxicosis Factitia** (ingestion of exogenous hormone) [1]. 4. **Statement 4 (True):** In Graves' disease, TSH-receptor antibodies (TRAb) stimulate the gland, leading to both hyperthyroidism and thyrotoxicosis [3]. 5. **Statement 5 (False):** This statement likely claimed that thyrotoxicosis and hyperthyroidism are synonymous or that all thyrotoxicosis requires antithyroid drugs (ATDs). This is false because conditions like thyroiditis are self-limiting and ATDs are ineffective as there is no excess synthesis [1]. **Why Option C is Correct:** It correctly identifies that while the terms are often used interchangeably in clinical practice, they are pathophysiologically distinct. Statements 1-4 accurately reflect this nuance. **NEET-PG High-Yield Pearls:** * **Radioactive Iodine Uptake (RAIU):** High in hyperthyroidism (Graves'); Low in thyroiditis or exogenous intake [1]. * **Most Common Cause:** Graves' disease is the most common cause of thyrotoxicosis worldwide [2]. * **Amiodarone:** Can cause both Type 1 (hyperthyroidism) and Type 2 (destructive thyroiditis) thyrotoxicosis. * **Treatment:** Propranolol is the first-line symptomatic treatment for most forms of thyrotoxicosis to control adrenergic symptoms [4].
Question 110: What is the most common presentation of endemic goiter?
- A. Hypothyroid
- B. Diffuse goiter (Correct Answer)
- C. Hyperthyroid
- D. Solitary nodule
Explanation: Explanation: 1. Why Diffuse Goiter is the Correct Answer: Endemic goiter is primarily caused by iodine deficiency. When iodine intake is insufficient, the thyroid gland cannot synthesize adequate amounts of thyroid hormones (T3 and T4). This leads to a compensatory rise in Thyroid Stimulating Hormone (TSH) from the anterior pituitary. TSH acts as a growth factor, causing hypertrophy and hyperplasia of thyroid follicular cells. Initially, this process occurs uniformly across the gland, resulting in a smooth, symmetrical, and diffuse enlargement (Diffuse Goiter) [1]. This is the body’s attempt to maximize iodine trapping and maintain a eumetabolic state. 2. Why Other Options are Incorrect: * Hypothyroid: While severe iodine deficiency can lead to hypothyroidism (especially in neonates as cretinism), most adults with endemic goiter remain euthyroid due to the compensatory enlargement of the gland. * Hyperthyroid: This is rare in endemic goiter unless a patient with a long-standing iodine-deficient goiter is suddenly given iodine (Jod-Basedow phenomenon). * Solitary Nodule: Endemic goiter is a generalized process affecting the whole gland. While it may progress to a multinodular goiter over many years due to repeated cycles of hyperplasia and involution [1], a solitary nodule is not the characteristic presentation. 3. High-Yield Clinical Pearls for NEET-PG: * Definition: A goiter is considered "endemic" if it affects >5% of the population (or >10% of children). * Progression: Diffuse goiter → Multinodular goiter (MNG) → Toxic MNG (Plummer’s disease) [1]. * Most Common Cause Worldwide: Iodine deficiency. * Most Common Cause in Iodine-Sufficient Areas: Hashimoto’s Thyroiditis. * Iodine Requirement: The WHO recommends a daily intake of 150 μg for adults.
Practice by Chapter
Diabetes Mellitus
Practice Questions
Thyroid Disorders
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Adrenal Gland Disorders
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Pituitary Disorders
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Calcium and Bone Metabolism
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Reproductive Endocrinology
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Lipid Disorders
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Endocrine Hypertension
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Multiple Endocrine Neoplasia
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Obesity and Metabolic Syndrome
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Neuroendocrine Tumors
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Endocrine Emergencies
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